How does HCC appear on US CT and MRI

How does HCC appear on US CT and MRI?

General: In the United States, more than 80% of patients with HCC have underlying liver disease (e.g., cirrhosis). Men are three times more commonly affected.

US: Appearance is variable, sometimes simulating metastatic disease. HCCs smaller than 5 cm are often hypoechoic, whereas larger lesions have mixed echogenicity. Fat within the tumor may cause internal hyperechoic foci. Vascular invasion is common; PV invasion is more common than HV invasion. Doppler US can depict tumor thrombus, which typically has an arterial waveform.

MDCT: On NCCT, HCCs are typically hypodense but may appear hyperdense in fatty livers, with 5% to 10% containing calcification. In the HAP, small HCCs (< 3 cm) typically demonstrate homogeneous and large HCCs heterogeneous enhancement, often with central necrotic areas of low attenuation. Imaging in the HAP allows detection of up to 30% more tumor nodules compared with NCCT and PVP imaging alone. In the PVP, HCC is usually iso- to hypodense in appearance. Even so, sometimes contour deformity, mass effect, or vascular, especially venous, invasion might be the only clues to detection. Hemoperitoneum, caused by rare spontaneous rupture, and intratumoral hemorrhage may also occur.

MRI: MRI can usually distinguish between regenerative nodules, dysplastic nodules, and HCC. HCC is usually hypointense on T1-w images, but HCC may be iso- or hyperintense depending on the degree of fatty change and internal fibrosis. Findings that suggest HCC include increased T2-w signal (in more than 70% of HCCs) and a diameter of more than 2 to 3 cm. A “nodule within a nodule” appearance (increased T2-w nodule within a decreased T2-w mass) is highly suggestive of HCC within a dysplastic nodule. Gadolinium-enhanced images increase the detection of HCC as HCC has marked enhancement in the HAP phase, late washout, and a peripherally enhancing pseudocapsule on PVP images. As the degree of malignancy increases, there is increased hepatic arterial and decreased portal flow to the nodules. HCC may also enhance after gadoxetic acid administration.

Both fibrolamellar HCC and focal nodular hyperplasia (FNH) have a central scar with multiple fibrous septa; however, fibrolamellar HCC has a high prevalence of calcification. The central scar in fibrolamellar HCC is typically T2-w hypointense and calcified, whereas in FNH the central scar is T2-w hyperintense and not calcified. Fibrolamellar HCC occurs at a younger age, has equal male to female incidence, and a better prognosis.


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